Pharmacotherapy to Manage Central Post-Stroke Pain.

Central post-stroke pain is a chronic neuropathic pain syndrome following a cerebrovascular accident. The development of central post-stroke pain is estimated to occur in 8 to 55% of stroke patients and is described as constant or intermittent neuropathic pain accompanied by dysesthesia of temperature and/or pressure sensations. These pain and sensory deficits are within the area of the body corresponding to the stroke lesion. The onset of pain is usually gradual, though it can develop either immediately after stroke or years after. Given the diversity in its clinical presentation, central post-stroke pain is a challenging diagnosis of exclusion. Furthermore, central post-stroke pain is often resistant to pharmacological treatment options and a clear therapeutic algorithm has not been established. Based on current evidence, amitriptyline, lamotrigine, and gabapentinoids should be used as first-line pharmacotherapy options when central post-stroke pain is suspected. Other drugs, such as fluvoxamine, steroids, and Intravenous infusions of lidocaine, ketamine, or even propofol, can be considered in intractable cases. In addition, interventional therapies such as motor cortex stimulation or transcranial magnetic stimulation have been shown to provide relief in difficult-to-treat patients.

Hepatic epithelioid hemangioendothelioma associated with acute disseminated encephalomyelitis by a possible paraneoplastic process.

Epithelioid hemangioendothelioma (EHE) is a low-grade, malignant vascular neoplasm that frequently involves the liver, lungs, bone, and soft tissue. Although not commonly associated with a paraneoplastic syndrome, paraneoplastic syndromes in the setting of EHE have been reported. Acute disseminated encephalomyelitis (ADEM) is an acute, autoimmune, demyelinating disorder of the central nervous system that most commonly occurs after an infection or vaccination. We present the case of a 23 year old female who developed the acute onset of fevers, tremors, right sided hemiplegia, global aphasia, and incontinence of urine and stool. MRI demonstrated findings consistent with a demyelinating disorder and brain biopsy confirmed the diagnosis of ADEM. The patient's work up revealed multiple liver lesions which were biopsy proven EHE. This case report discusses the diagnosis and treatment of two concurrent rare disease processes and the possible association of the processes via a paraneoplastic syndrome.

Painful Myoclonus Triggered by Lateral Antebrachial Cutaneous Nerve Entrapment at the Brachioradialis Muscle.

Compression of the lateral antebrachial cutaneous nerve is a rare clinical entrapment syndrome often overlooked as an initial etiology of pain. We present a case of an episodic upper limb painful movement disorder (myoclonus) in a 16-yr-old adolescent girl with a remote history of a surgically stabilized supracondylar humeral fracture who was later found to have entrapment of the lateral antebrachial cutaneous nerve. The incidence of a painful myoclonus triggered by a peripheral nerve entrapment is unknown. Combining a history and physical examination, electromyography, nerve conduction studies, and ultrasound enabled us to make an accurate diagnosis that was confirmed by resolution of symptoms after surgical release. This study conforms to all CARE guidelines and reports the required information accordingly (see Supplemental Check list, Supplemental Digital Content 1, http://links.lww.com/PHM/A855).

Platypnea-orthodeoxia Syndrome in a Patient with Cryptogenic Liver Cirrhosis: An Elusive Cause of Hypoxemia.

Platypnea-orthodeoxia syndrome (POS) has been defined as shortness of breath and hypoxemia in the upright position that improves with dorsal decubitus. This is a rare disorder caused by right-to-left shunts due to a persistent foramen ovale or pulmonary arteriovenous malformations. Hepatopulmonary syndrome can present with POS in the presence of pulmonary vasodilation and pulmonary arteriovenous communications in patients with liver disease. We report a case where the diagnosis of POS was made incidentally in a patient with cryptogenic liver cirrhosis. After other causes of hypoxemia were excluded, the diagnosis of right-to-left pulmonary shunt was confirmed by late opacification of the left heart chambers seen in a transthoracic echocardiogram. Interestingly, computerized tomography (CT) of the chest with contrast demonstrated a very prominent pulmonary vascular pattern extending to the periphery of the lungs. POS is a rare cause of hypoxemia that requires a high level of suspicion, and exclusion of more common causes of hypoxemia.

Myasthenia gravis crisis coinciding with asthma exacerbation in a patient with recent heroin use: three causes of acute hypercarbic respiratory failure.

A 57-year-old woman with a history of asthma, hypertension and substance abuse disorder was admitted to the medical intensive care unit with hypercapnic respiratory failure. After the history was obtained, patient admitted heroin use earlier that day. The initial physical examination revealed right eye ptosis, diplopia, fatigability of neck flexion and extension. She also presented with wheezing and a prolonged expiratory phase. Pupils were 4 mm, with sluggish response to light bilaterally. CT chest with contrast showed a large mediastinal mass. Three different processes coexisted in this patient: simultaneous occurrence of a myasthenia gravis crisis, asthma exacerbation and a component of heroin use. This case highlights a series of overlapping clinical features that could lead to potential confounding and misdiagnosis. Respiratory symptoms improved after initial treatment for asthma exacerbation, but ptosis, diplopia and fatigability of neck muscles persisted.

Transstomal small bowel evisceration after colonic perforation secondary to ischemic colitis.

Intestinal stomas are commonly used in a temporary or permanent fashion in gastrointestinal surgeries. The complication rate of stomas has been reported to vary between 23 and 50%. There is only one case in the literature involving transstomal small bowel evisceration following colonic perforation. In this paper, we aimed to present a patient with a perforated colon secondary to ischemic colitis, which resulted in small bowel evisceration through this perforation site.

Gastric outlet obstruction due to duodenal bezoar: A case report.

INTRODUCTION: Gastric outlet obstruction (GOO) is a clinical syndrome characterized by abdominal pain and postprandial vomiting. Causes of GOO include both benign and malignant disease. Bezoars, concretions of undigested or partially digested material in the gastrointestinal tract, are a rare entity and GOO due to duodenal bezoar is an uncommon presentation. PRESENTATION OF CASE: We report the case of a 56-year-old woman who presented to the emergency department acutely with a 3-day history of epigastric pain, weakness and postprandial nonbilious vomiting. Initially, an upper gastrointestinal endoscopy (UGE) was performed to evaluate the cause of the GOO. A solid impacted bezoar was detected in the first portion of the duodenum with complete obstruction of the pyloric canal. In spite of multiple attempts for fragmentation using different devices, the extraction attempts failed. We administered acetylcysteine and cola per os. Abdominal computerized tomography was obtained and showed a solid mass in the duodenum. UGE was performed once more however, the mass was not suitable for fragmentation and removal. Thus, surgical treatment was decided. The bezoar was extracted via gastrotomy. The postoperative period was uneventful. DISCUSSION: Even if a duodenal bezoar is small, because of its location it may cause GOO with abruptly clinical features. The diagnostic approach is similar to the other causes of the GOO. However, therapeutic options differ for each patient. CONCLUSION: We should remember all the therapeutic and diagnostic options for a patient with upper gastrointestinal bezoars who present at the hospital whether or not there is a predisposing risk factor.

Expression of calcium binding proteins in mouse type II taste cells.

It is well established that calcium is a critical signaling molecule in the transduction of taste stimuli within the peripheral taste system. However, little is known about the regulation and termination of these calcium signals in the taste system. The authors used Western blot, immunocytochemical, and RT-PCR analyses to evaluate the expression of multiple calcium binding proteins in mouse circumvallate taste papillae, including parvalbumin, calbindin D28k, calretinin, neurocalcin, NCS-1 (or frequenin), and CaBP. They found that all of the calcium binding proteins they tested were expressed in mouse circumvallate taste cells with the exception of NCS-1. The authors correlated the expression patterns of these calcium binding proteins with a marker for type II cells and found that neurocalcin was expressed in 80% of type II cells, whereas parvalbumin was found in less than 10% of the type II cells. Calretinin, calbindin, and CaBP were expressed in about half of the type II cells. These data reveal that multiple calcium binding proteins are highly expressed in taste cells and have distinct expression patterns that likely reflect their different roles within taste receptor cells.